HickOnACrick

As of yesterday, baby has continued to wean slowly on HFNC. FiO2 needs are mostly <40% on 3 LPM. Most importantly, baby has started bottle-feeding. We were very concerned about oral aversion. Baby remains on caffeine, multivitamin with iron, and Pulmicort NEB BID. Baby is gaining weight on a mixture of EBM and Neosure. When we have a baby that seems to be failing on HFNC, we generally move them over to NBCPAP or NIPPV, but we have used increased LPM flows (>5 LPM) on occasion. I have colleagues in other NICUs that prefer using HFNC at 6-8 LPM vs NBCPAP. We conducted surveillance PCRs on all staff that had a significant exposure to the family. We assigned the baby as a one-to-one nurse assignment so that nurse only cared for one baby. Baby has since come out of isolation. No other babies became symptomatic during this time, so no other babies have been tested for VRPs.

I use NaCl or NaAcetate in TPN. I can't remember the last time I used NaPO4. It is an option, but we do not use it often. We do not routinely check electrolytes until day 2-3, nor do we routinely add any supplements other than Ca and protein the first 2 days. What is happening with the weight of your babies that experience this hypernatremia? What about the urine output? A low UOP and substantial weight drop could imply lack if intravascular free water.

Here is our initial fluid management strategy: <750 grams = 120 mL/kg/day 750 - 1000 grams - 110 mL/kg/day 1001 - 1500 grams = 100 mL/kg/day We use 0.25 or 0.5 Normal saline in our UAC lines, running at 0.5-1 mL/hr. We do not routinely see hypernatremia in the first week, transient hyponatremia from immature renal function seems more common to us. Outside of the UAC fluids, our babies do not see Na in their maintenance fluids until 2-3 days of life. Hope this helps

We have had 4 confirmed subgaleal hemorrhages (SH) in the past couple of months. We have long suspected that many caputs have an element of SH, but avoid CT imaging due to the radiation and that identifying a SH will not change our management in most cases, if the baby is otherwise doing well. Of the 4 recent cases of SH, 2 have had more severe intracranial bleeding (intraventricular and subdural hemorrhages) and skull fractures - one of which was depressed. One of the cases was clearly in need of further head imaging on admission, due to the clinical picture, but the other was much more occult. This seems to be the crux of the problem - suspected occult subgaleal hemorrhage. Is imaging necessary to confirm? Each of these confirmed SHs had one thing in common - a drop in the Hct by at least 20%. The more severe cases experienced the drop earlier than the occult, less severe, SHs (12 hrs vs 48 hrs). Of the 4 cases, none required fluid resuscitation for hemorrhagic shock. With respect to the original questions: 1- Do you obtain brain image in every suspected SH? Not routinely. 2- Do you obtain brain image in clinically apparent SH in the abscent of neuro symptoms? I do now, especially if the Hct is dropping, or there is thrombocytopenia or coagulopathy. Skull radiographs may be enough to elicit a depressed skull fracture, which has possible implications in management. 3- Do you usually manage small SH in the newborn nursery until discharge home, if the baby remains clinically stable? Probably dependent on comfort level with your local nursery, but no, I would not feel comfortable if a known SH was in the nursery, unless the NICU had been consulted.

Going off service for a week, so an update. Baby has continued to slowly improve. Baby is now on HFNC 4LPM with oxygen needs around 30%, remains on full enteral feeds, fortified, and is gaining weight again. We may need to prolong the steroid course. As the course has weaned, baby's FiO2 needs have increased slightly (we have had the baby as low as 25% FiO2). The most recent chest radiograph shows improved expansion and aeration. Fibrosis and chronic changes are not the worst we have seen. We would not define the most recent CXR as being consistent with cystic BPD. We have spoken to a number of larger NICUs. This scenario (caretakers spreading C19 to NICU babies) is being seen in areas of the country where the incidence of C19(+) in the general population is the greatest. We have counseled our other families, especially those with the most fragile babies, that their social/work life needs to be a bubble of sorts.

I have found a few case reports about NICU graduates with BPD being admitted to PICUs with Covid-19. However, I have yet to find a case report of a former ELBW infant, who is still in the NICU, acquiring SARS-CoV-2, and deteriorating as a consequence. With regards to publishing, well, that is in part why I started this thread. It seemed like I was observing a novel effect of a novel virus, but wanted to see if others were seeing it as well. I reached out to my local University NICU's Medical Director, and they have not seen it in their NICUs. I have a couple other calls in to other large centers, but am awaiting their response(s). I plan to get IgG and IgM ELISA next week, considering whether it's worth testing mom's milk for virus and/or antibody. My local support for academic endeavors is greatly limited (county hospital), so I would welcome a collaboration if one has access to a more robust academic infrastructure. The baby's FiO2 needs are slightly higher today (35-40%). Work of breathing is better today, but baby remains dependent on the backup rate on NIPPV (currently set at 35 bpm). I have tested this daily by decreasing the rate at bedside. Baby continues to ride the rate and quickly desaturates if rate is weaned. A rate of 25 led to SpO2 of 70%. This, along with some increased irritability have me slightly concerned about neurologic sequelae. Thus far, his cranial ultrasounds have been clear - even for PVL. Baby is not receiving any sedation that would interfere with respiratory drive. The last blood gas was typical of a BPD baby - a mostly compensated respiratory acidosis - thus I believe the CO2 is available to drive respirations. We have discussed whether to do an LP every day for the past 5 days, but we do not feel the baby is clinically stable enough for that yet. Echo yesterday was unchanged from about 2 weeks ago - PFO with mild PHN. Function looks good. We are not routinely obtaining blood gases or radiographs. Prior to NIPPV, while on 5 LPM HFNC, baby had significant atelectasis, low volumes, and chronic changes. We plan for a repeat chest radiograph tomorrow to track changes, if any. Most recent CBC has trended toward neutropenia, but the ANC was still ~2500. We started more frequent and prolonged tummy-time today. I guess the kids call that "proning" these days We have considered chest physiotherapy, but worry the baby will not tolerate cup percussions. Baby remains on full feeds and oral dexamethasone, caffeine, MVI, and midazolam as needed. We lost IV access, and although it makes us nervous to not have access, we do not have a need for an IV right now. Caffeine dose is 5 mg/kg BID. At this time, we are using the DART protocol for dexamethasone. We made this decision based on our comfort level with using this regimen. However, if the FiO2 need continues to increase, we may need to rethink the dose. By limited accounts, it seems in PICUs they are using a dose about 4x the starting DART dose. It seems about once per year, we have cared for a former ELBW baby, that has never left the NICU, and acquires a viral respiratory pathogen and has clinical viremia. We are day 4 of severe symptomatology with this baby. We understand that some adult covid patients have a "honeymoon" period, lasting for 7-10 days, then can acutely become critically ill. By our experience with other VRPs, this is about the time we expect slow but continued improvement. Overall, we are trying to balance the baby's ex-premie with BPD needs with the additional support for his suspected Covid. Thus we have continued to limit blood draws, maximize nutrition, minimize radiation, continue the MVI, etc.

We also use: (weight in kg x 3) + 9 + length of cord This gives us an approximation of UAC depth. Half of UAC length approximates UVC depth. We use an AP radiograph to confirm placement. There is a method by which one can use the cardiorespiratory monitor to determine position of the UVC. Essentially you set the monitor to give an auditory beep with each heart beat. Advance the UVC until the frequency of beeps decreases (this implies the tip of the UVC is at the SA node), then pull the UVC back about 1/2 cm and it should be in a pretty good position. However, those I have seen use this technique still confirm with chest radiography. I would like to gain experience in POCUS as it might limit exposure to radiation.

Most I have worked with, including myself, will begin TPN as soon as possible in VLBW and ELBW babies, even with babies that have evidence of metabolic acidosis. In the larger babies, we are more likely to start a "clear" solution of trophamine, dextrose and calcium, or even just a straight dextrose solution - initially. To control blood glucose levels, mostly we can get by with just adjusting the IV rate until we can order a new bag of TPN (once daily). If adjusting the rate is not working (or we have reached a rate we are not comfortable with), we will "Y-in" an appropriate dextrose solution. Once we get glucoses under control, we will note the GIR at which that occurred, and tailor our TPN accordingly the next day. Long ago, I worked with some that would add an insulin drip to control high glucoses. I rarely see this being done anymore. My personal experience with insulin drips, especially in ELBW and VLBW babies, is that it is very difficult to predict how a baby will react. Insulin drips make for a long night of glucose checks, frequent adjustments to the GIR, adjustments to the insulin drip, and boluses of glucose. I suspect this unpredictability is exacerbated by insulin's adsorption to IV tubing. On insulin drips, I have seen glucoses vary between <20 and >200 without making a single change in GIR or insulin drip. I have yet to order an insulin drip, but have needed to manage them when ordered by others, thus my comfort level with insulin drips is minimal. In extreme hyperglycemia when we are already using D5W (in TPN) but still need volume, I have added insulin directly to the TPN. This seems to have a more predictable response. We are cautious with enteral feeds when we suspect an anoxic/hypoxic event, or in any baby with significant, or worsening, metabolic acidosis. In these babies, we generally assure renal and hepatic function are normal or substantially improving prior to initiating enteral feeds. Ultimately, it seems that the sooner we can begin enteral feeds, even if only small/trophic volume like 15-20 mL/kg/day, the sooner the blood glucoses become stable. Someone smarter than me can probably explain why, but I suspect intracellular signaling induced by enteral feeds, somehow stabilizes insulin production in the baby. Hope this helps,

Former 27 weeker, 895 gram male (now 1700+ and 36 and 6/7). STAT C-section for abruption, Apgars 1/3/5. Suspected antepartum anoxia/hypoxemia based on blood gases. Developed renal failure, elevated transaminases, etc. Very difficult respiratory mgmt, at 2 months of life, still on 5LPM HFNC and 50% FiO2 which is far outside the norm for us. This weekend, increased frequency and severity of apnea prompted a septic workup, including viral respiratory panel by RT-PCR. Negative for all the common resp viruses (including RSV, metapneumo, and flu), negative blood culture (now day 3), but positive for SARS-CoV-2. Tested mother, negative at admission, positive now. We are conducting surveillance on all staff, but right now it looks like he got it from mom. Mom now admits to some nausea and pharyngitis last week when the baby started becoming acutely ill. Mother is a healthcare worker and has not been vaccinated. Baby has moved from HFNC to NIPPV +6 and a backup rate of 35. He is dependent on the backup rate. His fiO2 need has decreased to about 30%. We started dexamethasone 2 days ago. He also had/has mild PHN as evidenced on echo last week and clinical lability. His only meds include caffeine, midazolam prn, dexamethasone, and multivitamin with Fe. We kept him NPO for about 24 hrs when he was most acutely ill, but as of this morning, he is back on full feeds. He received 48 hrs of nafcillin and gent this weekend. By my research, this is the first case of a former ELBW baby acquiring and becoming symptomatic with SARS-CoV-2 in the NICU. Has anyone experienced, or know of similar cases? If so, any special considerations for management? Is there the possibility of delayed severe symptomatology as is reported in the adult population?

Sad day. In spite of our best efforts, we have been unable to get this baby to ventilate and oxygenate. This morning, on a MAP of 10.5, this was the CXR: Last night we tried a mixture of milrinone and dobutamine to increase cardiac output and open the pulmonary vascular bed, but this made our oxygenation and ventilation worse. We stopped those meds and the baby did fairly well overnight with respect to his blood gases, and we were able to wean the amplitude somewhat. The echo yesterday showed a small PFO shunting left to right, but otherwise, no significant pathology. Throughout the morning and the afternoon, his oxygen saturation and ventilation worsened, necessitating we increase his amplitude to levels higher than last night. This was a CXR from the early evening: As compared to yesterday, the PIE has gone from micro to macro, and the hyperexpansion remains in spite of modest MAPs. This CXR was on a MAP of 11, amplitude of 32 and a Hz of 6. Baby was on 100% FiO2 and saturations were in the 60s. During the course of this disease process, I have been retrospectively reviewing the train of events. The mother was admitted with bulging bags at 23 weeks gestation, and in labor. Her labor was stopped with MgSO4 and indocin. She received a full course of betamethasone and was started on antibiotics soon after admission. Baby delivered vaginally a week later, within intact membranes and was intubated in the delivery room. All resuscitation was performed, surfactant administered, lines in place, antibiotics started, and the top of the isolette was down within 60 minutes. Looking at the PiPs, they dropped to low 20s after surfactant, but then began rising again at about 16 hrs of life. The FiO2 was between 21-25% during this time and the MAPs on volume-targeted ventilation (5 mL/kg) remained at around 7 mmHg. PEEP was at 5 mmHg. At 16 hrs of life, the PiPs climbed to the high 20s/low 30s. Because the supplemental FiO2 need was minimal, a second dose of surfactant was not given. Retrospectively, I can see evidence of PIE as early as the second day of life. My question today was: should we be basing our administration of surfactant less on FiO2 and MAPs and more on PiPs? Any thoughts?

Here is the CXR when the baby's MAP was 12: Here is the CXR when the MAP was 8: Clearly the hyperexpansion and air trapping are much worse on the second CXR with a lower MAP. Per @Miguel Pantoja we increased the MAP from 8 to 10 and have now weaned to 80% with SpO2 in the low 90s. We will continue to wean FiO2 until we reach a nadir, then slowly increase the MAP to a maximum of 12, while trying to wean the amplitude, then we will try and be patient and let the lungs heal if oxygenating and ventilating reasonably well. Ideally, I would like to get the amplitude to no more than 2x the MAP. I have a CXR ordered for the early morning and will try and post it hear to show the difference. Truly thankful for everyone who has contributed to this thread.

We started steroids 5 days ago, albeit the low-dose DART protocol of dexamethasone. I am about to start Milrinone and dobutamine to improve cardiac function. Thanks for your input.

We got the Hz down to 6, but our first attempt to wean the amplitude resulted in a pretty significant respiratory acidosis. What is really strange is that in spite of weaning the MAP from its original 14 to now 8, the hyperexapnsion by CXR is getting worse. I speculate that the air leak is not healing at all, and we essentially have thousands of little tension pneumothoraces surrounding what little areas of gas exchange the baby has; I wouldn't really call them alveoli at 24 weeks. Awaiting an echo now to assess shunting and see if an argument can be made to increase contractility with milrinone.

You may already be doing all of the following, but these are some of the things we do to prevent CLABSI: 1. TPN changes are performed as a sterile procedure; nobody is allowed within 10 feet of the bedspace without hat and mask. The RN doing the change is gowned up, hat, mask and sterile gloves. Of course, new tubing with every change of TPN 2. Standardized feeding guidelines to prevent days with a CVL in place 3. Minimizing breaks into the line for medications. Medications such as caffeine are changed to po as soon as baby demonstrates ability to tolerate po feeds (at about 60 mL/kg/day) 4. Changing from a UVC to what we call a "midline" if we anticipate the need for access beyond 5 days. A midline uses the same equipment/procedure as a PICC, but is not inserted all the way into a central vein. We treat theses as PIVs with respect to osmolarity/osmolality of TPN. Our last CLABSI was a baby who had a mild bloodstream infection which we identified as the same clone of bacteria we found in mother's EBM, but since the baby had a CVL in place, it was classified as a CLABSI - this was last year. We are not a huge NICU, but in general, about 30% of our census has had a CVL in place at some time. Based on our VON reporting, we regularly go more than one year without a reported CLABSI.

Thank you everyone for your input. In spite of continuing to lower the MAP, the CXR remains hyperexpanded. Base deficit slowly worsened throughout the day, although BP remained acceptable. The Hct is stable at 45%. I gave 20/kg of isotonic bicarbonate last night for a base deficit of -10, and the pH and base deficit improved. Awaiting another CXR this morning, if it still looks hyperexpanded, I will focus more on decreasing Hz. There seems to be some disagreement in what limited literature I can find (mostly opinions) as to whether a Hz of 12-15 or Hz of 6-9 is more beneficial. Anecdotal only, but this baby seems to be responding better to the low Hz strategy. I will get a bit more aggressive about lowering Hz today, then maybe I can start weaning the amplitude as I speculate it may be the culprit of hyperexpansion. I have used the HFJV in the past to manage PIE, with good results, certainly a much more rapid response than the current case I am managing. However, at my current facility, we do not have a HFJV. Also, we are using the SensorMedics HFOV, which to my knowledge, does not have the ability to do HFOV+VG. As to repositioning the baby, we tried this earlier this week with abysmal results. Repositioning on the SensorMedics HFOV is very difficult. I will give an update in an hour or two.